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. 2024 Dec 6;265(1):26–40. doi: 10.1002/path.6366

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© 2024 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Schematic synthesis of data and hypothesis. Organoids from nonadenomatous (NA) and adenomatous (A) biopsies displayed different phenotypes during investigations, summarized as delayed maturation in intestinal primitive cells from NA and overactive proliferation and migration in A organoids. Delayed maturation in intestinal primitive cells from NA seems to impact secretory differentiation (ATOH1 pathway) and may be linked to APC and LGR4 dysfunctions as well as to p110α activation. In the proliferation and migration of intestinal primitive cells from A, in addition to APC dysfunction, EGFR, and TGF‐β (TGF‐β), but probably also LGR5‐ and Wnt‐dependent pathways, play a critical role by regulating p110β, β‐catenin, and YAP. Notably, both NA and A areas differ in their survival pathways. APC*, mutant APC. Figure created with BioRender.com